代谢性酸中毒提示可能存在一些基础疾病。动脉血 pH 值<7.35 为酸中毒。血浆碳酸氢根水平降低和/或血清阴离子间隙(anion gap, AG)显著升高提示代谢性酸中毒。
代谢性酸中毒的原因可能有:
添加的强酸被碳酸氢根缓冲并消耗碳酸氢根离子
碳酸氢根离子经体液流失,通常经胃肠道或肾流失
非碳酸氢盐溶液快速补充到细胞外液中。
欲鉴别代谢性酸中毒的原因,需先计算血清 AG。血清 AG 等于主要阳离子钠(Na+)测量值减去主要阴离子氯(Cl-)与碳酸氢根(HCO₃-)测量值之和。
正常血清 AG 是由硫酸根(SO₄2-) 、磷酸根(PO₄-)、白蛋白和有机阴离子等未测量阴离子与钾(K+)、镁 (Mg+)、钙(Ca2+)等未测量阳离子之间的差值引起的。血浆蛋白也对维持正常血清 AG 发挥一定作用。[1]Dubin A, Menises MM, Masevicius FD, et al. Comparison of three different methods of evaluation of metabolic acid-base disorders. Crit Care Med. 2007 May;35(5):1264-170.
http://www.ncbi.nlm.nih.gov/pubmed/17334252?tool=bestpractice.com
急性代谢性酸中毒可持续数分钟至数天,在危重患者中相对多见,报道的发病率从更重度酸中毒的 6%(血浆 pH 值 <7.20)到最高达 64%。[1]Dubin A, Menises MM, Masevicius FD, et al. Comparison of three different methods of evaluation of metabolic acid-base disorders. Crit Care Med. 2007 May;35(5):1264-170.
http://www.ncbi.nlm.nih.gov/pubmed/17334252?tool=bestpractice.com
[2]Jung B, Rimmele T, Le Goff C, et al. Severe metabolic or mixed acidemia on intensive care unit admission: incidence, prognosis and administration of buffer therapy. A prospective, multiple-center study. Crit Care. 2011;15(5):R238.
https://www.doi.org/10.1186/cc10487
http://www.ncbi.nlm.nih.gov/pubmed/21995879?tool=bestpractice.com
[3]Kraut JA, Madias NE. Treatment of acute metabolic acidosis: a pathophysiologic approach. Nat Rev Nephrol. 2012 Oct;8(10):589-601.
https://www.doi.org/10.1038/nrneph.2012.186
http://www.ncbi.nlm.nih.gov/pubmed/22945490?tool=bestpractice.com
[4]Gunnerson KJ, Saul M, He S, et al. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Crit Care. 2006 Feb;10(1):R22.
https://www.doi.org/10.1186/cc3987
http://www.ncbi.nlm.nih.gov/pubmed/16507145?tool=bestpractice.com
持续数周至数年的慢性代谢性酸中毒则少见得多,但在老年人中随着慢性肾病的增加,其发生频率可能会增加。[5]Kraut JA, Madias NE. Metabolic acidosis: pathophysiology, diagnosis and management. Nat Rev Nephrol. 2010 May;6(5):274-85.
https://www.doi.org/10.1038/nrneph.2010.33
http://www.ncbi.nlm.nih.gov/pubmed/20308999?tool=bestpractice.com